ACVAA cheat sheet

Anesthetic depth is judged by a composite of reflexes (palpebral, laryngeal, pedal), jaw tone, eye position, and autonomic signs; no single reflex is reliable across species or drug protocols.

MAC is the alveolar concentration at 1 atmosphere that prevents movement in 50% of subjects to a supramaximal stimulus; MAC is not an ED50 for any specific procedure and varies with species, age, temperature, and concurrent drugs.

MAC-sparing effect: co-administration of injectable anesthetics, opioids, or alpha-2 agonists reduces inhalant requirement; typical reductions are 20-50% depending on drug and dose.

Isoflurane MAC is approximately 1.3-1.6% in dogs and 1.6-2.0% in cats; sevoflurane MAC is roughly half that of isoflurane (about 2.1-2.6% in dogs), so vaporizer settings are not interchangeable.

Minimum alveolar concentration is inversely related to body temperature and to age in neonates; hypothermia and young age both reduce MAC and increase risk of relative overdose.

Preoxygenation with 100% oxygen for 3-5 minutes before induction raises functional residual capacity oxygen stores and prolongs safe apnea time, particularly in brachycephalic or critical patients.

A properly functioning circle system delivers fresh gas flow near metabolic oxygen consumption (about 5-10 mL/kg/min) when the CO2 absorber is active; low-flow techniques reduce agent waste but require leak and absorber checks.

Capnography waveform (phase I inspiratory, II ascending, III alveolar plateau, 0 expiratory) is the standard for confirming tracheal intubation and detecting esophageal intubation, disconnection, or obstruction.

Recovery should be monitored until the patient can maintain sternal recumbency with intact airway reflexes; extubation timing depends on return of swallowing and jaw tone, not on a fixed clock.

Multimodal analgesia combines drugs acting at different sites (peripheral transduction, dorsal horn sensitization, descending modulation) to reduce individual doses and side effects.

NMDA receptor antagonists (ketamine at subanesthetic doses, ~0.5 mg/kg IV) attenuate central sensitization and opioid tolerance; they are adjuncts, not sole analgesics.

Opioid receptor pharmacology: mu agonism produces the principal visceral and somatic analgesia; buprenorphine is a partial mu agonist with high affinity and ceiling effect; butorphanol is a kappa agonist/mu antagonist with short duration.

NSAIDs act by cyclooxygenase inhibition; COX-1 is constitutive (gastric mucosa, renal blood flow, platelet function) while COX-2 is largely inducible at sites of inflammation; COX-1 sparing reduces but does not eliminate gastrointestinal and renal risk.

Local anesthetics block voltage-gated sodium channels; they are weak bases and are less effective in acidic infected tissue; maximum dose limits (e.g., bupivacaine ~2 mg/kg, lidocaine ~4-6 mg/kg in dogs) must be calculated before infiltration.

Pain assessment is species- and context-specific: validated tools include the Glasgow Composite Measure Pain Scale for dogs and the Feline Grimace Scale; physiologic variables alone are insensitive.

Alpha-2 agonists (dexmedetomidine, medetomidine) provide analgesia via alpha-2 adrenoceptor activation in the dorsal horn; bradycardia and vasoconstriction are predictable, and effects are reversible with atipamezole.

Tramadol provides analgesia through mu agonism and monoamine reuptake inhibition; oral bioavailability and efficacy vary widely among species and individuals.

Preemptive analgesia given before the noxious stimulus reduces central sensitization and subsequent analgesic requirements compared with treating pain after it is established.